|
KMID : 0376619920170040287
|
|
Seoul Journal of Psychiatry
1992 Volume.17 No. 4 p.287 ~ p.299
|
|
|
N-Methyl-D-Aspartate Receptors, Their Functions and Clinical Implications
|
|
|
|
|
Abstract
|
|
|
Recently, new interests in physiologic and pat-hophysiologic roles of excitatory amino acid receptors have been increasing with advances in research on their properties.
Excitatory amino acid receptors are classified into NMDA, Kainate, and Quisqualate receptor in accordance with each agonists showing characteristic electrophysiologcal response, and among these receptors, NMDA receptor is well characterized owing
to the
discovery of its specific and selective antagonists.
NMDA receptor is a complex consisting of NMDA recognition site, modulatory sites, and ion channel. All of these three dom9ains have an effect on final outcome of stimulation of NMDA receptors. Glutamate is the most important endogenous ligand to
NMDA
receptor.
NMDA ion channels have a high permeability to Ca++, but Ca++ influx through NMDA channels has to require postsynaptic neuronal depolarization. NMDA receptors are allowed selectively to amplify non-NMDA receptor-mediated synaptic response.
This unique physiological property of NMDA receptors is closely related to ong-term potentiation known as a physiological model of memory and learning.
@ES Clinical implications of NMDA receptors are as follows:
@EN First, hyperactivity of NMDA receptor might be related to the mechanism of pathogenesis of epilepsy. Second, neurotoxictiy of excitatory amino acids through NMDA recepors might play an important role in the pathogenesis of not only acute
disease
conditions, for exampe, ischemic or hypoglycemic brain damage, but also chronic neurodegenerative diseases such as Alzheimer's and Huntington's disease. Finally, one of the biological models of schizophrenia, the PCP model, is based on the
hypothesis
that glutamatergic neurotransmission might be decreased due to dysfunction of NMDA receptors as compared to amphetamine model, and may permit the development of new mechanism of pathogensis and treatment strategies for schizophrenia.
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|